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The coronary circulation is unique among vascular beds, as myocardial perfusion depends not only on aortic pressure, conduit artery patency, and microvascular resistance but also on the dynamic interaction between myocardium and microvasculature during the cardiac cycle. As a result of phasic compression and decompression of intramyocardial vessels by surrounding myocytes, coronary flow is intimately linked to myocardial relaxation and contraction, a process known as cardiac–coronary coupling.

Although the dual effects of the distal intramyocardial pump and proximal changes in aortic pressure were demonstrated in animal models several decades ago (1), recent developments have provided a powerful tool capable of characterizing these effects in humans. It is now possible to simultaneously measure intracoronary pressure and flow velocity during cardiac catheterization by using a Doppler and pressure sensor–tipped 0.014-inch guidewire that closely resembles the characteristics of a conventional coronary guidewire. These measurements can be used to perform wave intensity analysis (WIA), providing information on the origin and nature of wave energy that drives or impedes coronary flow.

Parker and Jones (2) proposed WIA as a novel approach to analyzing cardiovascular hemodynamics, based on studies of gas dynamics during World War II. In a coronary artery, forward-traveling waves arise from the aorta and are associated with congruent changes in flow and pressure; when pressure rises, flow increases and vice versa. Backward-traveling waves originate from the intramyocardial microvasculature and are associated with opposite changes in flow and pressure; when pressure falls, flow increases and vice versa. These waves can be further classified according to their effect on coronary flow (accelerating or decelerating) or pressure (compression or expansion). Davies et al. (3) first applied WIA in the human coronary circulation and described 6 distinct waves, 4 of which have been consistently found by others since that study. The backward compression wave (BCW) is a distally originating wave that arises during isovolumetric contraction (at the onset of systole) and decelerates coronary flow. The forward compression wave is a proximally originating accelerating wave that reflects transmission of rising aortic pressure in early systole. The forward expansion wave arises proximally, decelerates flow, and reflects the slight fall of aortic pressure in late systole. The backward expansion wave, the main driver of flow in the normal coronary circulation, originates distally due to decompression of the microvasculature in early diastole.

During the decade since its first description in humans, WIA has been used to study cardiac coronary–coupling in patients with valvular and ischemic heart disease (4–6). It has recently been shown that perfusion efficiency improves during exercise in the healthy heart, as the relative increase in accelerating waves is greater than the increase in decelerating waves (7). However, in contrast to the healthy heart, perfusion efficiency decreases with exercise and hyperemia in patients with aortic stenosis (AS), as the decelerating wave energies increase more than the accelerating waves, primarily due to a marked increase in the BCW (due to greater compressive forces on the microvasculature in systole) as well as an attenuated rise in forward compression wave (reflecting the effects of AS on the rate of rise in aortic pressure). Immediately after transcatheter aortic valve replacement, accelerating wave energies are seen to increase before any appreciable changes have occurred in resting or hyperemic microvascular resistance (8). These observations suggest that abnormal coronary coupling, rather than changes in microvascular function, is responsible for symptoms of angina in AS.

In this issue of the Journal, Raphael et al. (9) report an elegant application of WIA in patients with hypertrophic cardiomyopathy (HCM). Thirty-three patients with HCM and 22 control subjects with structurally normal hearts underwent simultaneous Doppler flow velocity and distal coronary pressure measurements in the left anterior descending artery. The decelerating BCW was larger in magnitude and comprised a greater proportion of total wave energy in patients with HCM than in control subjects. The BCW was of longer duration in the subgroup with left ventricular outflow tract obstruction; interestingly, coronary flow reversal was seen in approximately two-thirds of HCM patients with left ventricular outflow tract obstruction but not in control subjects. The ratio of accelerating to decelerating waves was lower in patients with HCM compared with patients with structurally normal hearts (1.9 ± 2.0 vs. 3.3 ± 1.4); with hyperemia, the ratio fell further. Their findings firmly implicated systolic compression of the intramyocardial microcirculation as the main impediment to coronary flow in HCM.

Remodeling of intramural arterioles is frequently found in HCM and has been postulated to be the main determinant of blunted coronary flow reserve, with the implication that resting and minimal microvascular resistance are increased in these patients (10). In keeping with previous studies, Raphael et al. (9) found that coronary flow reserve in the left anterior descending artery was lower in the HCM group than in the control group. However, resting microvascular resistance was lower in the HCM group due to compensatory vasodilation. Consequently, there was reduced vasodilator reserve, with no difference between groups in minimal microvascular resistance or maximal (hyperemic) flow rate. Increased coronary flow at rest in HCM is likely to be a response to increased demand, although it is impossible to estimate the latter from the current data because there was no direct measure of oxygen consumption or wall stress. Hence, cardiac coronary–coupling seemed to be the key determinant of impaired myocardial perfusion in HCM, rather than increased microvascular resistance, a major shift in our understanding of coronary hemodynamics in this condition. It is interesting that traditional mechanistic concepts have also been recently challenged with regard to coronary flow in AS.

Coronary WIA offers great potential for unraveling the physiological basis of cardiac disease states characterized by altered myocardial mechanics, microvascular dysfunction, or both, as well as for evaluating the effect of pharmacological and mechanical therapies for these conditions. Studies using WIA in patients with left ventricular dysfunction have already provided unique insights into the mechanism of action of intra-aortic balloon counterpulsation (11) and cardiac resynchronization therapy (12). However, a few caveats should be mentioned. Measurement of coronary flow velocity in the cardiac catheterization laboratory can be challenging, and a learning curve exists to ensure accurate and reproducible data collection. Significant improvements could be made to existing Doppler wire technology that would make data acquisition easier and more reliable but until a clinical utility has been identified, manufacturers are less inclined to invest in developing these wires. In addition, although WIA outputs are clinically intuitive, their underpinning principles are complex; with an ever-expanding range of conditions in which WIA is used, it will become important to return to these basic principles and ensure that inherent assumptions remain appropriate (13).

Furthermore, several steps exist between acquisition of raw Doppler velocity and pressure data and the derivation of final wave profiles. Each is time-consuming, introduces operator bias due to manual selection of raw data, and involves offline analysis using software custom-made by each academic center that specializes in this technology. The process needs to become quicker, more automated, and standardized before WIA can be used in large-scale multicenter trials and translated into routine clinical practice. Finally, it requires invasive cardiac catheterization, and the development of noninvasive techniques to derive some or all of such powerful data would be welcome (14).

Footnotes

↵∗ Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.

Dr. Perera has reported that he has no relationships relevant to the contents of this paper to disclose.

(2012) Improvement in coronary blood flow velocity with acute biventricular pacing is predominantly due to an increase in a diastolic backward-travelling decompression (suction) wave. Circulation126:1334–1344.

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